Heart rate–mediated blood pressure control in preterm fetal sheep under normal and hypoxic–ischemic conditions

Background: The understanding of hypoxemia-induced changes in baroreflex function is limited and may be studied in a fetal sheep experiment before, during, and after standardized hypoxic conditions. Methods: Preterm fetal lambs were instrumented at 102 d gestation (term: 146 d). At 106 d, intrauteri...

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Veröffentlicht in:Pediatric research 2013-04, Vol.73 (1-4), p.420-426
Hauptverfasser: Zwanenburg, Alex, Jellema, Reint K., Jennekens, Ward, Ophelders, Daan, Vullings, Rik, van Hunnik, Arne, van Pul, Carola, Bennet, Laura, Delhaas, Tammo, Kramer, Boris W., Andriessen, Peter
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Sprache:eng
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Zusammenfassung:Background: The understanding of hypoxemia-induced changes in baroreflex function is limited and may be studied in a fetal sheep experiment before, during, and after standardized hypoxic conditions. Methods: Preterm fetal lambs were instrumented at 102 d gestation (term: 146 d). At 106 d, intrauterine hypoxia–­ischemia was induced by 25 min of umbilical cord occlusion (UCO). Baroreflex-related fluctuations were calculated at 30-min intervals during the first week after UCO by transfer function (cross-spectral) analysis between systolic blood pressure (SBP) and R–R interval fluctuations, estimated in the low-frequency (LF, 0.04–0.15 Hz) band. LF transfer gain (baroreflex sensitivity) and delay (s) reflect the baroreflex function. Results: Baseline did not differ in LF transfer gain and delay between controls and the UCO group. In controls, LF gain showed postnatal increase. By contrast, LF gain gradually decreased in the UCO group, resulting in significantly lower values 4–7 d after UCO. In the UCO group, LF delay increased and differed significantly from controls. Conclusion: Our results show that intrauterine hypoxia–ischemia results in reduced baroreflex sensitivity over a period of 7 d, indicating limited efficacy to buffer BP changes by adapting heart rate. Cardiovascular dysregulation may augment already present cerebral damage after systemic hypoxia–ischemia in the reperfusion period.
ISSN:0031-3998
1530-0447
DOI:10.1038/pr.2013.15